Let's get started because I have lots of information to share with you and I know there will probably be a lot of questions and I want to make sure I give you some time for questions. Welcome to this session, Managing Antiplatelet and Anticoagulant Drugs Like a Pro. My name is Nina Abraham. I'm from the Mayo Clinic in Arizona and I also run, I think, the nation's only cardio-gastro neurology clinic. So over the last 25 years I've had the opportunity to not only publish a lot in this space but also discover some strategies that are pro-tips that I hope to share with you that you can take home and start using immediately in your practice. I would ask that you silence your phones if you have ringers on and do feel free to take photos of any slides. I know a lot of speakers don't like that but I realize there will be a lot of practical tips here that you may have not heard before. So let's start by mentioning that I absolutely have no disclosures. And that's important because there are a lot of folks in spaces where we talk about medications who have conflicts of interest with drug companies. Over the last 25 years I have not worked with any drug companies for the reason being that I want to be able to tell you the truth. And I want to try and disentangle from you some of the myths, the urban legends and some of the voodoo around this topic so that you have some pragmatic strategies that you can use immediately in your practice. I'm going to focus on what you really want to know. Whenever I give lectures on this topic this is really the stuff that clinicians ask me to review. We're going to talk about the acute GI bleed management, specifically how to reverse, interrupt and resume antiplatelet and anticoagulant drugs. I'm also going to mention hemostatic techniques because there's a lot of confusion about what the right strategies are or the best strategies for managing GI bleeding in patients who are going to need to be on chronic anti-thrombotic drugs. I'm going to talk briefly about post-polypectomy bleeding management and prevention since that's the bulk of what most community gastroenterologists are doing in the United States. I'd also like to spend some time talking about iron deficiency anemia and how to manage those patients with the recurrent anemias that you're going to see. PEGS and anti-thrombotic agents is a hot topic because if you've ever been on call or on staffing your hospital service, inevitably you're going to get a call about a PEG and a patient who is on these drugs. And finally, I'd like to share with you some common errors that increase bleeding and thromboembolism. And just by stopping to do these common errors, you can keep yourself out of the crosshairs with a lawyer in the future. So let's start with a case. This is one of my patients who is a weekend hiker. I live in Scottsdale, Arizona where there are a tremendous number of beautiful mountains. So if any of you are coming to the American College of Gastroenterology meeting in Phoenix in the fall, I encourage you to get out hiking. But don't do what my patient did. This was a 76-year-old gentleman with ischemic heart disease, atrial fibrillation on a Pixaban and aspirin 81 milligrams a day. He hiked Camelback Mountain and this is my pro tip for those of you who want to hike Camelback Mountain. It is actually very, very tough. So if you're not conditioned to do it, you might want to pick something a little less challenging when you're in Phoenix. He took a whole bunch of NSAIDs to deal with his aches and pains and then presented to our emergency room feeling faint and dizzy. His hemoglobin had dropped a fair bit from his known baseline. He was a cardiac patient at our institution so we know what it was just a few months prior. He was tachycardic and hypotensive. The emergency room stabilized him with three units of Paxil's fluids and he became hemodynamically stable. So this is your typical anticoagulant, antiplatelet bleeder that you're going to see in the emergency room. And there are some important elements that are raised by this case that I'd like to bring to your attention. The first is a change in clinical paradigm. The first thing you need to do in any patient who's having an anticoagulant bleed is first assess whether or not they're having a life-threatening hemorrhage or not. And that's because the management strategy differs based on whether or not the patient is having a life-threatening hemorrhage. So how do you identify the patient with a life-threatening hemorrhage? Well these are the folks who have major clinically overt or apparent GI bleeding with hypovolemic shock and severe hypotension requiring pressors or surgery. These are the people who they can't stabilize in the emergency room and they're transferring to an ICU. And then they follow what I like to call the rule of fives. There's a decrease in hemoglobin of greater than five grams per deciliter or they've required more than five units of red blood cells to be transfused. There's something very important about that threshold and that's because when you look at clinical studies in the cardiac literature, once a patient has had hemorrhage that is that significant, their risk of mortality goes up exponentially. These are the patients who are at risk of having death caused by their bleed. Why is it important to identify the patients who are having a life-threatening hemorrhage? It's because in those patients you should be considering the use of a reversal agent. Now my patient was on a Pixaban and did not quite meet that threshold for a life-threatening hemorrhage and more importantly, they were able to stabilize this gentleman in the emergency room. Now this is not the patient who I'd be reaching or advising the emergency room physician to use a reversal agent. So what would, if this patient had been in that category of a life-threatening hemorrhage, what would be the appropriate reversal agent for him? Well if you talk to the drug reps, they're going to push and dexonate alpha. And this drug is readily available even though it has very little GI bleed data to support its use. But what concerns me the most about this agent is that it has a very high risk of thromboembolism. Now all the thromboembolism studies and drug reversal studies use the comparator fresh frozen plasma. Not that you should be using that, we're going to be talking about that a little later. But that is the gold standard comparator. Fresh frozen plasma has a risk of thromboembolism of 7 to 8%. And dexonate alpha's risk of thromboembolism is anywhere between 12 to 30% depending on your dose. Now when this drug was first approved by the FDA in the United States, it used double the dose that is now required. And that's where we saw those 30% thromboembolism rates occurring with the use of this drug. Now it's about 12 to 15%, which is still very, very high. And much higher than the gold standard accepted rate. The other thing that concerns me about this drug is it's extremely expensive. When it first became available, it was over $42,500 per person for use per dose. Now it's half that because the company now has appreciated that you can use half the dose for the same effect. But certainly if the patient has a life-threatening hemorrhage and they have taken rivaroxaban or epixaban within the last 24 hours, you could consider using this agent. If the patient had been on dabigatran, the agent to use is idarocizumab. This is a very good reversal agent. It's safe and it's very effective. And it is not associated with a very high thromboembolic risk at all. It's about 5 to 6%. Currently, most of the Americans who are being prescribed direct oral anticoagulants are being prescribed epixaban or rivaroxaban. So unless you work in the Kaiser Permanente system in California, you're probably not seeing a lot of dabigatran. Some hospital systems are now requiring cardiologists and primary care doctors to start patients on dabigatran because of the cost differential between that and the factor Xa inhibitors, rivaroxaban and epixaban. So if you are in a system where dabigatran is regularly used and you have a patient with a life-threatening hemorrhage, you can reach idarocizumab with good effect. But I want to introduce you to prothrombin complex concentrate or PCC. We're going to talk about PCC in relation to warfarin bleeding in the next few slides. But I want to share with you some data that's now been released. At the time we wrote our 2022 guideline on this topic, we only had two cohort studies with comparator arms. There are now many, many more, both the GI literature as well as the cardiology literature and the neurology literature showing that PCC may actually be the better choice in the setting of a life-threatening hemorrhage of patients on direct oral anticoagulants. And that's because it acts a bit like an Allen key. It has multiple areas of impeding the clotting cascade. So it has multiple targets for activity. And what it's been shown to be very effective in doing is reversing the anticoagulant effect of patients on direct oral anticoagulants as quickly as within two hours, which is what you would expect to see in patients who were getting PCC to reverse warfarin. So when it comes to warfarin, it's really important that you stop using fresh frozen plasma. A lot of you are still using FFP, and that is no longer recommended by any of the national GI societies, the cardiology societies, and even the hematology societies. And that's because it takes large volumes of FFP to be transfused very slowly in a patient who has a warfarin supratherapeutic bleed that may be at that life-threatening hemorrhage levels, so that patient in whom you want to think about reversing. And it takes almost eight units of FFP to just minimally change a supratherapeutic INR. And it comes with a risk of transfusion-associated complications, specifically pulmonary edema and congestive heart failure, which is why the American Society of Hematology has endorsed and gone on to say it should not be used for the reversal of warfarin effect in patients with hemorrhage. So what is the choice? Here again, it's four-factor prothrombin complex concentrate, or PCC, which contains factors 2, 7, 9, and 10. So it acts in multiple locations in the coagulation cascade. And that is, again, your first choice for the reversal of a warfarin supratherapeutic bleed. Now, if you compare the 22 guidelines to the 2016 guidelines, you'll notice that we no longer endorse the use of vitamin K. And that's simply because vitamin K just does not work fast enough. And we have more than adequate good evidence from the literature to show that in a setting of an important life-threatening hemorrhage caused by warfarin, you need to get in there and do endoscopy quickly, within 24 hours. And it's going to take more than 24 hours to reverse that INR that is supratherapeutic in a patient if you choose vitamin K. Now remember, you do not need to normalize an INR to be effective in hemostasis with a warfarin bleed. Even a modestly elevated INR, anything less than 2.5, has been shown in many studies of hemostasis to be all that you need to ensure no re-bleeding events. So don't wait to normalize the INR. Once your INR gets to 2.5 or less, you're good to go. Last slide about the management of anti-platelet bleeds. There's been a number of really important court cases that have gone through at the risk of physicians where platelet transfusions have been given for major GI bleeds as well as intracerebral hemorrhage bleeds. And we now know, not only in the GI literature, but also in the neurologic literature and following cardiovascular surgery, that if you give routine platelet transfusion in patients who are on anti-platelet drugs, drugs like Plavex or Prazugrel or Clopidogrel or Brylinta, you actually increase the risk of death by almost five-fold. And the fact that that pattern is seen over multiple disciplines in the response to multiple types of bleeding is concerning. But it isn't surprising. And that's because platelets are an active substance. And when you transfuse them inappropriately, you activate an entire cytokine cascade that then leads to that patient's death. So the American Guidelines, which I've had the pleasure of being the author of every single one that's ever been published, does not endorse a threshold level for the use of when you should be considering platelet transfusion. Our colleagues in Europe, specifically Britain and the ESGE, do suggest that a platelet threshold of about 100,000 is where you could consider transfusing. Now the Asians have a lower threshold at 50. We debated this at length around the table. And we had the premier thrombotic expert in the United States and Canada on our guideline committee. And the point is, we don't know what the level is. So it really is a guess. But we appreciate that there are individual clinical situations where patients may be significantly thrombocytopenic. And as part of your strategy for GI bleeding, you may need to provide them with platelets. In that situation, we always recommend that you have a multidisciplinary discussion. And most importantly, make sure you include the patient in a shared decision-making manner. Because there is a well-documented increased risk of death associated with platelet transfusion in these patients who are getting antiplatelets. One thing that we're seeing less of but still occurs is the interruption of cardiac aspirin in anticipation of endoscopic management for a GI bleed. What do I mean by cardiac aspirin? This is aspirin dosed at 81 milligrams in the United States, 76 milligrams in Europe, or 325 milligrams in other countries in patients prophylactically for the prevention of heart attack and stroke. This is secondary cardiac prevention. These are people who've already had a heart attack or stroke. This is not the patients who are taking it as primary prevention because they saw an advertisement on television asking them if their aspirin strategy might be right for you. The American College of Family Medicine, the American College of Internal Medicine, as well as emergency medicine all in the U.S. as well as in Australia and Europe has now moved away from the use of aspirin for primary prevention in cardiac patients. Because it has been shown not to be effective and comes with a very high risk of GI bleeding. But if that patient is on aspirin strategy because they've already had a heart attack or a stroke, you do not and you should not stop that cardiac aspirin. Because we know from our colleagues in Hong Kong that when you stop that aspirin in the anticipation of doing a hemostatic procedure, you actually increase that patient's risk of death. Hemostasis is very easily and adequately achieved on cardiac aspirin. So do not stop it because you take away from that patient that morbidity, mortality benefit. Let's talk about hemostatic methods. There is this urban myth that it's not safe to use thermal hemostatic methods in patients on antiplatelets and anticoagulants. And I want to reassure you now that it is perfectly safe to use Gold Probe or APC in patients on anticoagulants with a modestly elevated INR, so 2.5 or less. And it's also okay to use in patients on antiplatelet agents with appropriate temporary interruption of the drug. There is no increased risk of bleeding after the use of thermal therapy and there are excellent results for hemostasis. So do not be afraid to use that. If the lesion that you're wanting to address would be better suited by using a thermal method because of its location or your ease of access, both in terms of equipment or location of the bleeding source, go ahead and use that thermal therapy. Now when it comes to APC, you should be very comfortable using APC in cardiac patients because any patient who has ischemic heart disease has turbulent flow in their arteries and capillaries. Okay, that's the atherosclerosis. And wherever you're going to have turbulent flow, you're going to have an increase in the formation of arteriovenous malformations. That's why you see so many AVMs in cardiac patients, anywhere from the stomach straight through to the anus. And they tend to recur because we have no way of going in with a roto-rooter and removing all that atherosclerotic plaque. Cardiologists can try and decrease further plaque from forming by managing blood pressure and cholesterol levels, but you can't really dissolve the plaque that's already there. So since the gut is so richly perfused for its other purposes of transporting nutrients elsewhere in the body, we do see a lot of AVMs. When you see an AVM in a cardiac patient, whether or not it's bleeding, I would encourage you to pull out your APC catheter and eliminate it. Why? Because this will change the clinical course of a patient who needs chronic anticoagulant and antiplatelet therapy. They're the patients who come back with the obscure occult GI bleeding. They're the patients who come back for assessment because of chronic iron deficiency anemia. And when I get sent these patients in my clinic for second, third and fourth opinions, I always go through the old endoscopy reports. And without fail, I'll see AVM, non-bleeding AVM noted in the colon, non-bleeding AVM seen on capsule endoscopy, none of which were addressed. And when we go back and we address them, the patient's out of the woods with their chronic anemia. Now, my preferred strategy for managing mucosal disruptions in an acute GI bleed in a patient on antithrombotic drugs is mechanical hemostasis. If you have good technique with mechanical hemostasis, whether it's an over-the-scope clip or a mechanical clip, you will achieve excellent results. And the reason why I like this modality is there's no concern of an eschar that will slough off and then a delayed re-bleeding event. With good, well-placed mechanical clips, you can restart that patient on their antithrombotic agent immediately. And remember, that's really what's going to be life-saving for the patient is the resumption of their drug. But the problem with mechanical hemostasis, as we all know, is sometimes you find bleeding lesions that are not in a location that is amenable to a well-placed clip. In that situation, I would recommend you go with thermal therapy. Let's talk about the efficacy of clips for patients on antiplatelets and anticoagulant drugs. There are very few studies that have been done on this topic in this patient population. But there is one from Germany. It's a very small study where 76% of patients were on these drugs, anticoagulant and antiplatelet drugs. And they achieved 100% primary hemostasis. The vast majority of the lesions were ulcers in this study. But what I found particularly interesting was the re-bleeding rate. It's 35%. And you say, well, what's the big deal about that? That's the same re-bleeding rate you see in through-the-scope clips. And it's not so much the choice of through-the-scope versus over-the-scope clips that matter. It's the technical adequacy of the placement of the clip. In all cases where you see that 35% increase in re-bleeding rate, it's because there was incomplete approximation of the edges, the loss of the clip during the procedure, or a mistake that I see often with clip placement, which is you put a clip on top of an inherent thrombus without knowing what's underneath that clot. You don't know if there's a visible vessel there or if you're actually in the right area for approximating the edges if you just stick the clip over the clot. And so when that happens, that's a very frequent reason why clips fail in these patients. And then you resume them on their drugs and then they have that re-bleed. And then the other technical point that I would point out to you is when you put your clips on, especially an over-the-scope clip, you're probably using a bear claw type clip, you want to make sure that the vessel is not close to the teeth. The whole point is to approximate the edges and bring them together in that clamp. And so the vessel's in the middle and gets that full mechanical hemostatic tamponade. If you do not place your clip properly and you have the teeth on the vessel or close to the vessel, you'll just increase the risk of re-bleed once you resume the antiplatelet or the anticoagulant. So what about malignant bleeding in patients on these drugs? A lot of patients with malignancies have high thrombotic risk, so they are started prophylactically on anticoagulants. So we now know in terms of malignant bleeding that the use of hemostatic sprays are very, very effective as monotherapy. We used to think of them as temporizing measures and then get them to an IR or to a tertiary center where more definitive therapy can be done. Now we know they are very effective in the monotherapy setting. I'm only showing you one of the six randomized control trials that have since been published on this topic because I want you to note that in this study as well as most of them, very few patients were actually on antiplatelets and anticoagulants. So we don't actually know how effective hemostatic powder sprays are for malignant bleeding in patients on these drugs yet. I do know of a number of groups around the world who are working on this particular topic, so that will help clarify things. Hopefully they will be as effective in patients on antiplatelets and anticoagulants as they are in the other patients who are having malignant bleeds without the additional burden of the antithrombotic drug. Let's talk about resuming drugs. For warfarin, which has been around on the market for over 90 years, there is a remarkable lack of studies on the right timing of warfarin resumption. There are none in the GI literature of good quality. So when we did our grade process for our most recent 2022 guideline, we had to go to the neurologic literature, cardiovascular literature, and the cardiovascular surgery literature. And what's the take-home message? If you resume warfarin within four to seven days of its initial discontinuation, it is associated with a very low risk of thromboembolism. In the few endoscopic studies that exist, that risk of thromboembolism is only 1%. So when I say this, I always hear physicians say, what happens if they rebleed? Well, if they rebleed, you go back in and you deal with what you've got. I always tell my patients, it's a lot easier for me to deal with a post-polypectomy bleed or a post-initial hemostasis bleed for a GI bleed than it is for me to explain to you why we held your warfarin and then you had that big stroke, all right? So you do not want to delay resumption of warfarin because of your fear of resumption of a bleed, because we know how to take care of GI bleeds. If anything, we have a lot more tools in our toolbox to deal with GI bleeds than we had at the time many of these poor quality endoscopic studies were done. What about direct oral anticoagulants? Well, there's no high certainty evidence in the GI bleed setting, but there is very good quality evidence in the elective setting, and that is you should be resuming direct oral anticoagulants the day after your procedure. And so when we actually were writing this guideline, the author of the premier trials on direct oral anticoagulants and thrombosis and procedural management was actually the thrombosis expert on our panel. And so he was very, very kind to release the GI-specific literature to us, the GI-specific data points, which had not been analyzed separately from their large international study. And Alan Barkin and I did do that analysis, and we published that in the Red Journal, the American College of Gastroenterology Journal, in 2022. That showed that using a standardized approach of stopping the anticoagulant 24 hours before you do the endoscopic strategy and resuming it the day after was associated with a very low risk of re-bleeding of only 2.5% and less than 1% risk of thrombotic effects. And that was shown across all of the procedural low-risk procedures of which endoscopy falls into in this large international study. So that I think is something that has made things easier for us. You can protocolize your management now in terms of a temporary interruption and resumption of direct oral anticoagulants. Let's move on to polypectomy. This is a 71-year-old female with a mechanical valve on warfarin. She had surveillance colonoscopy done by one of my colleagues with the removal of a 2.5 centimeter polyp at the hepatic flexure using cold snare EMR. Warfarin was appropriately held five days before the planned procedure, and she was bridged with low molecular weight heparin, which would be appropriate given her mechanical valve. The next day, they restarted her on her warfarin, and she had profuse hematochezia. She had a five-gram drop in hemoglobin, and she landed up in the emergency room. PCC was given because she was having a significant GI bleed, and urgent colonoscopy showed this non-bleeding visible vessel at the site of the prior polypectomy at the hepatic flexure. So before we talk about the polypectomy dos and don'ts, I want to bring your attention to the bridging. I had said that this patient was appropriately bridged with low molecular weight heparin, and that's because she had a mechanical valve. But there are actually very few patients who do need to be bridged. So if you are bridging automatically, I want you to know that we have two large randomized control trials in the cardiac setting, as well as five good quality observational studies in the GI setting showing that routine low molecular weight heparin bridging during discontinuation or temporary interruption of warfarin is associated with a very high risk of post-procedural bleeding without conferring any protective cardiac benefit, except in the patients in that second box. You should be considering low molecular weight heparin bridging in patients with mechanical valves, like my patient, patients with CHAD scores that are very high. So atrial fibrillation with CHAD scores greater than five. This is an important question to ask in your endoscopic practice. Any patient who has a history of thromboembolism with previous temporary interruption of their warfarin, you need to know about that person, because they likely have other hematologic factors predisposing them to a prothrombotic state. So in those people, you should be bridging them. And certainly after certain large cardiovascular surgeries where there is a prothrombotic transient effect related to post-surgical factors, low molecular weight bridging is appropriate. But in most, you don't need to bridge these people when you interrupt the warfarin. So let's go back to our polypectomy. What's the current state of literature on anticoagulants and antiplatelet patients when it comes to polypectomies? And I see a lot of phones going up, and this is the slide I'd recommend you take a photo of, okay? Because I put it all on one slide, so you don't have to read a lot of studies. I put it in two columns, anticoagulant versus antiplatelet data, and this is both warfarin as well as direct oral anticoagulants. But I put them in two columns because I want you to see the patterns are the same. When it comes to either antiplatelets or anticoagulants, patients do better if they have temporary interruption before their planned polypectomies, okay? When compared to patients in whom the drugs are continued. The period of temporary interruption depends on the agent that the patient's prescribed. If it's a direct oral anticoagulant, as I previously mentioned, you're going to hold it the day before the procedure in most patients, unless you're planning to do big EMRs or ESDs, large mucosal disruptions, when you're going to need to hold it for two days before the procedure. Warfarin still gets held five days before, and unless they're in one of those categories of patients at high risk of clot, you don't need to bridge. Same thing holds true for antiplatelet drugs. If the patient is on clopidogrel or ticagrelor, you should be holding that drug for five days before the procedure, and if they're on prazugrel, which is the only agent that requires a seven-day hold, you always continue the cardiac aspirin, the aspirin that's been prescribed for secondary prevention. Using that strategy of temporary interruption, and specifically timed temporary interruption, your postpolypectomy bleed is less than 2%, very, very low. And we had studies published in the last two years that showed that in the anticoagulant side of the equation, patients who were prescribed Apixaban over Rivaroxaban or Warfarin actually had the lowest postpolypectomy bleed rate, so it was lower to 1% than 2%. The other thing I want to show you is that the thromboembolism rate associated with this strategy is very, very low. A lot of endoscopists who tell me, well, I'm worried about stopping the drug, so I'm just going to do all my polypectomies on the drugs, they worry about a falsely elevated concern about thromboembolism. Now I know you're going to go to the doctor's lounge and hear about the one guy who had the one patient. Every time I walk into our nurse practitioner PA area for internal medicine, I'm always getting asked this question. I heard about a guy who had his Warfarin held for one day and he had a big stroke. It's actually really, really rare, okay? And we have that in lots of data across GI, neurology, and cardiovascular medicine. So you can either practice medicine based on a heuristic in fear, or you can practice medicine based on what the data shows us. And we know that with an appropriate management strategy of the drug before your procedure and in the endoscopy setting, thromboembolism is less than 1%. When it comes to the anticoagulant, get the patient back on their drug the next day, all right? And the same is true as well for antiplatelets, unless there is a concern for immediate hemostasis. The only people in whom this usually tends to apply are the folks going for ESD, using EMRs where there's large, wide mucosal fields and perhaps the endoscopist wasn't as diligent about using the hot grasper to carefully go and cauterize any remaining vessels. But the point is you want to get these patients back on their antithrombotic agent because that's actually what's life-saving for these patients. We were purely the technicians to prevent the future risk of colon cancer. The immediate risk of them is cardiac death, and that is mitigated by the use of these drugs. There are some patients in whom you should be deferring elective polypectomy procedures and elective screening procedures, and those are patients who are in that risk window for very high risk of thromboembolism and cardiac side effects from drug manipulation. And that's 90 days from stroke, 90 days from TIA, and 90 days from pulmonary embolus or deep venous thrombosis, okay? That first 90 days is when all the bad cardiac juju happens that puts those people at high risk. So that's not the time to do the screening colonoscopy on the guy who has a history of polyps or a family history of colon cancer, okay? You say, come back to me in four or five months and then we'll take care of this. Because we do want you to do the temporary interruption, but we do not want you to put them at risk when they're at the highest risk of adverse cardiac events. When it comes to the antiplatelet side of the equation, you want to delay non-urgent screening 90 days from an acute coronary syndrome event and within three to six months of a drug-eluting stent. It used to be one year, no questions asked. But there have been some really important large randomized controlled trials in the cardiac literature showing that in the average patient who has bad coronaries and gets a couple of drug-eluting stents placed, you need a minimum of three months for continuous coverage of their dual antiplatelet therapy and usually a maximum of six months. And you will see if you're working in an environment where your cardiologists are really in tune and in step with best practice guidelines, that many of those patients who you saw with dual antiplatelet therapy six months ago will now be put on aspirin monotherapies or clopidogrel monotherapies after that window of time. That's actually where the field is moving for safety in terms of adverse events, both cardiac and GI. The good old days of seeing patients who are permanently on dual antiplatelet therapy only happens when the care of that patient has been sent back to the primary care doctor. They've not had follow-up with the cardiologist and you say, wow, your stent was put in when? 2015. Why are you still on dual antiplatelet therapy? And they're like, I don't know, my mind just keeps getting renewed. So it's important to question and know where the state of the cardiac literature is. Let's talk about the choice of cold snare versus hot snare. And if any of you have ever heard me debate this topic with Doug Rex, you know we have very different views and it's usually good natured antagonism. But I am now moderating my perspective on cold snare in this patient population because of some important studies that have come out since the last DDW two years ago when Doug and I were on a stage debating this topic. We now know that in patients on antiplatelets and anticoagulants, cold polypectomy techniques are very safe for polyps less than one centimeter. So that has become my new strategy, whereas I never used to embrace cold snare. I do cold polypectomies in all my patients on these drugs chronically if their polyps are less than one centimeter. Now we've had some very important studies published in the last year and a half on the benefit of cold snare polypectomy for polyps greater than one centimeter. The two most important large good quality trials, one from Australia and one from Germany. I'm going to show you the data from both. Now the message is the same in both. In both of these studies, 20 to 25% of these patients were on anti-thrombotic drugs. So it ticked the box for me in the sense that it actually showed me that enough of their subgroup had these drugs on board so it would give us a sense about safety. What you see in both studies is clearly the post polypectomy bleed rate is much lower in patients who had the cold technique versus the hot technique. But what concerns me more than the post polypectomy bleed rate is the recurrence rate because of the residual tissue that was left behind. And that again was shown in the chronicle trial from Germany. And so I think that really behooves us to make sure that if you are going to do cold snare polypectomy, you know how to do it correctly with a dedicated cold snare with the proper fried egg technique, which I see a lot of people just not knowing the difference of how to use a cold snare and take a polyp off that way versus the traditional hot snare. It's not the same way. You need to leave an edge of normal tissue around the lesion when you do cold snare polypectomy so that you do not risk residual tissue. We are currently, I'm currently participating in a large Delphi panel and study, international study to look at this particular topic led by folks you all know, Asma Shaukat, Heiko Pohl, et cetera, et cetera, all the big players in the field. But that's the take home message. It's all about how much adenomatous tissue you're leaving behind which predisposes that patient to the recurrent cancer or the interval cancer. Everyone gets worried about the post polypectomy bleed. But I would remind you, we can take care of a post polypectomy bleed, okay? Stop fearing the post polypectomy bleed. It's no biggie. What we can't take care of is the patient who goes home with a come back in seven to ten years because we took off your polyp and then they come back with a cancer. And it's far more common than you would like to know. I see at least two or three patients in endoscopy who have interval cancers. Polypectomy is done in my institution and elsewhere in the community. So just be aware of your technique if you're going to do cold polypectomies because technique really matters. Let's talk about prophylactic clipping. This important study by Spettacini in 2020 showed us that clipping large lesions on the right side is actually beneficial, all right, to decrease re-bleeding risk. And you'll remember my patient with the mechanical valve had her large cold snare polypectomy done in the hepatic flexure. So when this patient came to the inevitable M&M, you know, we had a big discussion about what should have happened and I immediately got asked, I said, you know, hindsight's 20-20 but we know that this patient had a lesion on the right side, had a large mucosal defect. Should you consider clipping the patient? And the endoscopist didn't because they had really drunk the tea on the safety of cold snare polypectomy. So I can assure you now that if you're taking off a large lesion on the right side, most of my colleagues at Mayo are prophylactically clipping. Now people say, well, clipping's really expensive. It is expensive in the United States. But in other countries, clips can cost as little as $184 U.S. And we know from cost-effectiveness studies that once the clip price gets to that level, it's actually what we call a dominant strategy. Preventively clipping all your big mucosal lesions actually saves the patient money and morbidity in the future. And that's assuming a base case of three clips put on for every large lesion. So I don't know where you practice, and I don't know how much your clip costs in terms of comparison to the U.S. dollar. But the closer under $250 per clip you are, the more routine I think clipping should be for large mucosal lesions. But definitely if you work in the U.S., do it on the right side because there's good evidence that it matters. All right, here's an important patient that I want to talk to about that brings up some important points. This is my patient with coffee ground emesis. He was on, the referral came from cardiology. Safety of triple antithrombotic therapy suspected GI bleed on vacation. This is a lovely gentleman who lived in Scottsdale, went out to visit his daughter in Colorado. He was on Eliquis, Plavix, and aspirin for cardiac disorders. He had squamous cell carcinoma and one of those serious radical neckectomies that E&T does, takes off everything, and has pretty much been subsisting on soup and food since his surgery about a year and a half ago. He was out visiting his daughter. He woke up from sleep coughing with blood and coffee grounds all over his pillow and was taken to the emergency room of the local small town in Denver, outside of Denver, Colorado. The wife was told that he had had copious amounts of coffee grounds by the EMS providers and he had a big bleed clearly from his labs. The local GI physician got really worried about the post-surgical anatomy and so deferred doing endoscopy and said, let's treat you conservatively and then get you right home to Mayo Clinic where they can deal with you. So he went back to see his cardiologist who eventually referred the patient to me and I actually saw him in my clinic a month after his acute GI bleed. But you can see what the labs were. I saw him literally on December the 31st, 2024. You can still see that his hemoglobin hadn't come back to normal. His maticrit was still low. And when I saw him in January, his bleed was December 31st, pardon me. When I saw him on January the 14th, I had his iron indices done the day before. You can see he's still very low in iron and his saturation is very low. So what's in your differential here? The important thing is to ask the additional questions and not just assume it's a GI bleed. And whenever you hear that story, you want to ask about epistaxis. Remember epistaxis is a very common cause of melanin and coffee ground emesis in this cardiac population. And sure enough, his wife, when I asked the question, said, oh yeah, within two hours of him being put on Plavix after his stent got put in, he had horrific nose bleeds that lasted four hours. And I said, has that ever happened again? Oh yeah, we've been in the emergency room multiple times and ENT has packed his nose multiple times. And I said, huh, interesting. And then we eventually did the endoscopy because that's what we're being paid to do and we didn't find anything interesting. Big surprise. So what do I do? I send him off. Oh, we're going to talk about Vitron C and protein supplementation for his iron stores. If you go to the inpatient session tomorrow, Monday afternoon, I'm doing this talk related to inpatient management and one of the big pearls is, remember, it takes four iron molecules to make one hemoglobin molecule. So looking at the full iron panel will tell you the chronicity of the GI bleed, if it is a GI bleed, as well as the severity of any nutritional deficiency. And putting a patient on something as easy as Vitron C daily can normalize a nutritional deficiency within three months. That's a big pro tip. But you'll hear more about that on Monday. All right, so he went out and had his boring GI workup, but a very interesting ENT workup. So suffice to say that this was never a GI bleed. This was epistaxis, horrific epistaxis that only got worse because he was at super high altitude outside of Denver hiking. And apparently the Kieselbach's plexus gets super dry and then it really bleeds like stink when you're on dual antiplatelet therapy. Even I learned a little something something from my ENT colleagues. So he's not had any more issues with GI bleeding. ENT is doing ENT-like things to deal with his nose. And he now has normalized his iron with appropriate nutritional supplementation. So here are my iron deficiency anemia pro tips after 25 years of seeing these patients. Here's another slide worth taking a photo on. Finding a treatable lesion is not as common as nutritional deficiency, especially in patients over the age of 65, all right. The American diet is terrible for iron-containing foods. And you need to be intentional about eating iron-containing foods. And if this patient's a cardiac patient, they've been told to avoid spinach and dark leafy greens. So they're really iron deficient. But what people forget are there are other excellent sources of dietary iron. Shellfish, 25 grams per serving. Dried fruits and nuts. Iron-fortified cereals. There are so many other ways to get iron into your diet, all right, other than spinach, kale, and collard greens, and red steak, okay. So just know how to take an iron, a nutritional history. All I say is, do you eat red meat, no. Do you eat spinach, collard greens, kale, no. When was the last time you ate, and then I go through the high-containing foods. And if it's the average American, I live on chicken and mashed potatoes. They're not eating iron, all right. They're going to have a nutritional deficiency component. Again, cardio GI patients are predisposed to have AVMs because of turbulent flow, whether it's through atherosclerosis or an LVAD or some other mechanical device that's been implanted. You will see these patients. It's super-duper common. And so I, again, reiterate the importance of treating non-bleeding AVMs with APC to prevent them from going down the rabbit hole of multiple negative studies being done because of iron deficiency anemia. If you have not met Vitron C and you are still giving ferrous sulfate or ferrous gluconate, please stop. A, that's a drug that only a primary care doctor should even be suggesting because we have more sophisticated options in GI. Vitron C is an iron and vitamin C complex tablet, which has been shown to be far more effective in comparative studies to the traditional oral over-the-counter agents, even if they take a vitamin C supplement. So A, that's important. B, it causes no dyspepsia, it causes no constipation, and it causes no black stool, right? So A, compliance is good. B, you can actually tell if the patient's having an obscuricultural oblique from dark stool as opposed to stained stools from their iron preparation. And as I previously mentioned, if you keep these patients on Vitron C taken daily, not three times a week, which a lot of people think is all you need, but for this indication, they will normalize their iron within three to four months if this is only nutritional deficiency. Let's talk very briefly about PEGs because I see we have about 10 minutes left. We've all seen this patient, the patient who's had the massive stroke, has gone through the massive workout, has been languishing on the floor for a week, and then all of a sudden they find a room placed for him in the rehab facility and it becomes an immediate emergency to get the PEG placed. Drives me crazy. Sure, it drives you crazy too. And for many years I got asked, what can we do about PEGs in these patients who are on these drugs? Well, I didn't have data for you up until last year. Now we know from this large network meta-analysis of over 8,000 patients that it is perfectly safe to put in a PEG on dual antiplatelet therapy. You do not have to hold that patient in hospital now to hold that thenapyridine agent for five days. There was no increased risk of post-procedural bleeding with dual antiplatelet therapy continuation when compared with no dual antiplatelet therapy or monotherapy of only aspirin or clopidogrel. So that's really important information, okay? So that's something you should take home from this meeting. What about anticoagulants? Hasn't changed. You will have more PEG bleeds if you do not temporarily interrupt your anticoagulant. All right? So if this patient's on Warfarin, that's a five-day hold. But if the patient's on a DOAC, you're lucky. 24 hours before your procedure, you tell them to hold their horses for one day, keep the bed warm in the rehab facility, and we'll put the PEG in tomorrow, and you can ship them out same day. Remember with interruption of Warfarin, you don't need to bridge most of these patients unless they fall into that category of very specific high-risk cardiac patients. And DOAC resume next day. So here are my take-home points. Feel free to take home slides, photos, because we all know we don't go back to the app to look at the slides. Come on. Who are we kidding? When it comes to an anticoagulant bleed, triage is really important. You need to know who meets the criteria for a life-threatening hemorrhage because it's in those patients you should be considering a reversal agent. Only in those patients because the inappropriate use of reversal agents actually increases the risk of thrombotic adverse events. Warfarin super therapeutic bleeds, you want to choose PCC with a life-threatening hemorrhage. It's cheap. It's cheerful. It's very effective. And remember, you don't have to normalize an INR to be successful with your endoscopic therapy. You can be successful even with a moderately elevated INR. And in cardiac patients, that's particularly important because when you go in there, in 83% of patients, you're going to find a high force class stigmata lesion, all right, in these life-threatening hemorrhages. And those need to be dealt with before the patient goes to the cath lab. The cath lab is actually what is life-saving for them. We merely are the temporizing measure to get them to the cath lab, okay? So make sure you take care of that. When it comes to DOACs, again, no routine reversal agents unless they meet that definition for life-threatening hemorrhage. And remember, you can now use PCC. You don't have to use one of the more expensive reversal agents. Prothrombin complex concentrate, factors 2, 5, 7, 9, and 10. I can't tell you the brand name, but you've got it at your hospital. Okay. Any platelet-related GI bleeding, stop, stop. Just walk away from the platelets, please. You're killing people, all right? There really is no good threshold level for when you should consider it. But if you are considering it, please have multidisciplinary discussions and shared decision-making with your patient. Thermotherapy is safe to use. So if that's your choice when it comes to GI bleeds, feel free to use it. Mechanical hemostasis, regardless of the choice you use, will still be associated with 35% pre-bleed risk, but it all depends on your technique. And we don't know enough about hemo sprays yet in this patient population to know if it will be as effective for malignant bleeding as it is for patients who are not on these drugs. But please, please, please, please, please, if you treat a patient with a GI bleed and they're going to be on chronic antiplatelet or anticoagulant therapy, make sure you put them on a PPI if they've not been put on a PPI long-term. And here's another pro tip. Before you start the oral PPI forever, make sure they poop in a cup so you can find out what the helicobacter pylori status is, because eradication of helicobacter pylori decreases your risk of post-aspirin, antiplatelet, and warfarin bleeding substantially too if they are eradicated. When it comes to polypectomies, go ahead with the cold polypectomies, but make sure you're doing it correctly so you don't have an interval cancer. Error on the side of clipping large mucosal defects, especially on the right side. And remember, iron deficiency anemia can be caused by other things, including turbulent flow, vascular actasias, and nutritional deficiency. So don't forget that. Don't just scope and run. PEGs, go ahead on dual antiplatelet therapy, but know that you will need to temporarily interrupt if they're still on an anticoagulant. And here are my slide, last slide I want you to take a photo on, because these are so commonly made. And I do not do medical legal work. Every year at DDW and ACG, I get mobbed by physicians who want me to speak out for them or their lawyers. I do not do that work, so I made this slide as a public service announcement, all right? These are the things that get you into trouble, routine use of a reversal agent, unnecessary use of platelet transfusions, discontinuation of cardiac aspirin, failure to promptly restart your antithrombotic agent once immediate hemostasis is achieved, and when all else fails and it looks like a gray area patient, have a multidisciplinary discussion so everybody's on the same page. Remember there's no tug of war between the heart and the GI tract. The heart always wins. Thanks for your attention. Have a great meeting.

antiplatelet management

anticoagulant drugs

hemorrhage assessment

GI bleeding

reversal agents

thromboembolic risks

cold snare polypectomy

dual antiplatelet therapy

nutritional history